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Am J Physiol Heart Circ Physiol 283: H837-H844, 2002. First published April 18, 2002; doi:10.1152/ajpheart.00789.2001
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Vol. 283, Issue 2, H837-H844, August 2002

Involvement of Na+/Ca2+ exchanger in endothelial NO production and endothelium-dependent relaxation

Jean-Christophe Schneider1, Driss El Kebir1, Christiane Chéreau2, Jean-Christophe Mercier3, Josette Dall'Ava-Santucci1, and A. Tuan Dinh-Xuan1

1 Service de Physiologie-Explorations Fonctionnelles and 2 Laboratoire d'Immunologie Biologique, Centre Hospitalier Universitaire Cochin, Assistance Publique, Hôpitaux de Paris, Université Paris 5, 75014 Paris; and 3 Service de Réanimation Pédiatrique, Hôpital Robert Debré, 75019 Paris, France

Endothelial nitric oxide (NO) synthase (eNOS) is controlled by Ca2+/calmodulin and caveolin-1 in caveolae. It has been recently suggested that Na+/Ca2+ exchanger (NCX), also expressed in endothelial caveolae, is involved in eNOS activation. To investigate the role played by NCX in NO synthesis, we assessed the effects of Na+ loading (induced by monensin) on rat aortic rings and cultured porcine aortic endothelial cells. Effect of monensin was evaluated by endothelium-dependent relaxation of rat aortic rings in response to acetylcholine and by real-time measurement of NO release from cultured endothelial cells stimulated by A-23187 and bradykinin. Na+ loading shifted the acetylcholine concentration-response curve to the left. These effects were prevented by pretreatment with the NCX inhibitors benzamil and KB-R7943. Monensin potentiated Ca2+-dependent NO release in cultured cells, whereas benzamil and KB-R7943 totally blocked Na+ loading-induced NO release. These findings confirm the key role of NCX in reverse mode on Ca2+-dependent NO production and endothelium-dependent relaxation.

monensin; signal transduction


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